Rosa Rubicondior: Malevolent Design - A Brilliantly 'Designed' Process For Spreading Influenza

Dead cells after the self-destruction and fragmentation process. The large green areas are the “eat me” signals which alert immune cells to kick-start clean-up and recycling process, while the small green circles are the “Footprint of Death” F-ApoEVs left behind by the dying cell.

’Footprint of Death’ gives new clues to cell life, News, La Trobe University

My previous post was about the discovery, reported in Cell Host & Microbe in May 2026, that a single amino-acid change in a coronavirus protein can alter how a bat-related coronavirus interacts with the immune systems of bats and humans. In the case of SARS-CoV-2, the virus that causes COVID-19, such changes help to explain how a virus that may be relatively benign in its natural host can become a serious pathogen when it crosses the species barrier into humans. By creationists' own criteria, this should qualify as intelligent design.

This post concerns another example which, if creationists applied their criteria for intelligent design consistently, would be further evidence of malevolent design. It is the finding, reported in Nature Communications, that influenza A virus can exploit part of the normal process of programmed cell death to help infect neighbouring cells.

Applied consistently, these discoveries would portray creationists' putative designer god as a malevolent entity that designs ways to increase suffering. But, since creationists need to portray this alleged designer as the omnibenevolent god of the Bible, this supposed 'evidence of intelligent design' somehow ceases to be evidence of design at all and becomes evidence of 'Sin' and 'The Fall', as creationists abandon any pretence of science and retreat into Biblical mythology to explain away inconvenient facts.

The discovery, by a team led by PhD candidate Stephanie Rutter in Professor Ivan Poon’s lab at the La Trobe Institute for Molecular Science (LIMS), shows how each step in the process of cell death and renewal is important in helping a dying cell break down and be cleared away by the body’s immune system. The team found that, as cells self-destruct, they change shape, lift away from their surroundings, and leave behind a residue which the researchers dubbed the 'footprint of death'. This contains a previously undescribed type of extracellular vesicle (EV). EVs are small packages used by cells to transport proteins, lipids, DNA and RNA to other cells, acting as an important means of communication between cells.

These new vesicles, known as FOOD-derived apoptotic extracellular vesicles, or F-ApoEVs, normally mark the site of a dead cell and help the immune system identify and clear away the remaining fragments, preventing inflammation and other harmful consequences. But this useful clean-up process can also be turned into a weakness. The researchers found that, when dying cells are infected with influenza A virus, viral proteins and even virus particles can be carried in these F-ApoEVs, providing another route by which infection can spread to neighbouring cells.

Had this process been beneficial to humans, rather than to influenza viruses, creationists would doubtless hail it as a marvel of intelligent design by their god. Yet, because the benefit is to a virus and the result can be disease, suffering and death, the same kind of complexity somehow ceases to count as evidence of design and is quietly reclassified as a mysterious consequence of 'The Fall'.

Creationists get into this bind because they are trying to force the evidence into their preferred mythology. Science has no such problem. The immune system, cell-death pathways and the pathogens that exploit them are all products of evolutionary history, not foresight. They are parts of a continuing arms race in which every useful biological process presents opportunities for parasites, viruses and other pathogens to exploit. An influenza virus that stumbles upon a weakness in a host system does not need to understand it, plan it, or design it; it merely needs to leave more copies of itself than viruses that did not.

Background^ Cell Death, Vesicles and Viral Opportunism. Cells in multicellular organisms do not merely die as isolated units. In many cases, they undergo apoptosis, a controlled form of programmed cell death in which the cell is dismantled in an orderly way and its remains are cleared away by immune cells. This helps prevent inflammation and allows tissues to renew themselves without leaving damaging cellular debris behind.

One part of this clean-up system involves extracellular vesicles (EVs) — tiny membrane-bound packages released by cells. These vesicles can carry proteins, lipids, DNA and RNA, and so act as messages or markers for other cells. In the La Trobe University study, researchers found that dying cells can leave behind a newly described type of EV at the site where the cell had been attached. They called this residue the FOotprint Of Death, or FOOD.

The FOOD vesicles, known as F-ApoEVs, appear to act rather like cellular breadcrumbs, marking the site of a dead cell and helping immune cells locate and clear away the remains. That is a useful, evolved process for maintaining healthy tissues. However, like many biological systems, it can also be exploited. The researchers found that, when cells infected with influenza A virus die, these vesicles can contain viral proteins and even virus particles, giving the virus another possible route to neighbouring cells.

In evolutionary terms, this is not evidence of foresight, planning or benevolent design. It is an example of biological opportunism. A normal cell-maintenance process creates an exploitable opening, and any virus variant that uses that opening effectively leaves more descendants. Natural selection then preserves the exploit, without needing intelligence, purpose or moral intent.

Glossary

Apoptosis: A controlled form of programmed cell death in which a cell is dismantled and cleared away without usually causing damaging inflammation.

Extracellular vesicle (EV): A small membrane-bound package released by a cell, often carrying proteins, lipids or genetic material to other cells.

FOOD: Short for FOotprint Of Death; the residue left behind at the site where a dying cell had been attached.

F-ApoEV: A FOOD-derived apoptotic extracellular vesicle; a newly described type of vesicle associated with the site of apoptotic cell death.

Phagocyte: An immune cell that engulfs and digests dead cells, debris or invading microbes.

Efferocytosis: The process by which phagocytes clear away dead or dying cells.

Virion: A complete virus particle capable of infecting a host cell.

Influenza A virus: A type of influenza virus responsible for many seasonal flu infections and some pandemics.

Pathogen: An organism or infectious agent, such as a virus, bacterium or fungus, that can cause disease.

The paper in Nature Communications was accompanied by a press release from La Trobe University:

’Footprint of Death’ gives new clues to cell life
Scientists at La Trobe University have discovered a previously unknown way viruses could spread around the body, potentially paving the way for more effective drug development.
The research, published in Nature Communications, uncovers new understanding of the process of cell death and renewal.

Led by PhD candidate Stephanie Rutter in Professor Ivan Poon’s lab at the La Trobe Institute for Molecular Science (LIMS), the research shows how each step in the process is critical to help a dying cell break down and be cleared away by the body’s immune system.

Researchers discovered that as cells self-destruct, they change shape, lift away from their surroundings, and leave behind a residue dubbed “the footprint of death” which contains a previously undiscovered type of Extracellular Vesicle (EV).

EVs are tiny packages released by cells to transport proteins, lipids, DNA and RNA to other cells, serving as a crucial mechanism for communication between cells.

The new EVs, known as F-ApoEVs, mark the site of a dead cell and serve as breadcrumb clues to help the immune system identify and clean up cell fragments, preventing unwanted inflammation.

But early tests on cells also revealed that when dying cells are infected with influenza, the virus can hijack the clean-up process by hiding particles inside the F-ApoEVs, which could aid the spread of infection to neighbouring cells.

Professor Poon, Director of the Research Centre for Extracellular Vesicles (RCEV), said the findings could have a big impact on future drug development.

Understanding this basic biological process could open new avenues of research to develop new treatments that harness these steps and help the immune system better fight disease. Billions of cells are programmed to die each day as a part of normal turnover and disease progression, and until now, it was believed that the cell fragmentation process during cell death was random and fairly simple. Our findings demonstrate the complexity of this process and highlight how each step in the process is actually critical to help the dying cell break down efficiently and to be cleared away by the immune system.

Professor K. H. Poon, co-senior author
Department of Biochemistry and Chemistry
La Trobe Institute for Molecular Science
La Trobe University
Melbourne, VIC, Australia

Lead researcher and PhD candidate Stephanie Rutter said the study demonstrated the importance of cell-to-cell communication to maintain health, and how these processes can be manipulated by viruses.

We know that the body clears away dead cell fragments to prevent them lingering and causing inflammation and autoimmune diseases such as Systemic Lupus Erythematosis (SLE), and we saw F-ApoEVs are readily cleared from the site of cell death. What we didn’t expect was how viruses can also take advantage of this process and cause infection by hiding in F-ApoEVs.

Stephanie F. Rutter, lead author.
Department of Biochemistry and Chemistry
La Trobe Institute for Molecular Science
La Trobe University
Melbourne, VIC, Australia

Researchers hope the discovery could lead to better understanding and eventually better therapies for infectious and autoimmune disease.
The more we can understand about cell death and what happens to cells after they die, the better we can understand disease pathologies and find new treatments..

Stephanie F. Rutter.

The study’s co-leader, Dr Georgia Atkin-Smith from WEHI, said that understanding how dying cells communicated within the immune system was critical, given the broad implication of cell death across many diseases.
This study has revealed that dying cells can continue to communicate from the grave and may impact immune function.

Dr Georgia K. Atkin-Smith, co-senior author
The Walter and Eliza Hall Institute of Medial Research
Parkville, VIC, Australia.

This research was conducted by scientists at La Trobe University’s RCEV, LIMS and the School of Agriculture, Biomedicine and Environment (SABE). The study was conducted in collaboration with researchers at WEHI and Toronto Metropolitan University in Canada.

Publication:
Rutter, S.F., Kang, T., Ryan, G.F. et al.
The formation of the ‘footprint of death’ as a mechanism for generating large substrate-bound extracellular vesicles that mark the site of cell death.
Nat Commun 16, 9160 (2025). https://doi.org/10.1038/s41467-025-64206-3

Abstract
Apoptotic cells communicate to phagocytic cells through releasing soluble factors and apoptotic cell-derived extracellular vesicles. However, whether there are additional factors that remain attached at the site of cell death to signal to phagocytic cells is currently unknown. Here we show that apoptotic cell retraction generates a membrane-encased, F-actin-rich ‘footprint’ tightly anchored to the substrate that marks the site of cell death, coined ‘the FOotprint Of Death’ or FOOD. Formation of FOOD is observed frequently across many different cell types, apoptotic stimuli and surface composition. Mechanistically, FOOD formation is regulated by the protein kinase ROCK1. 3D time-lapse microscopy studies revealed that FOOD vesicularises into distinct large extracellular vesicles. These extracellular vesicles expose the ‘eat-me’ signal phosphatidylserine and can function to ‘flag’ the site of cell death to neighbouring phagocytes for efferocytosis. Under a viral infection setting, FOOD can harbour viral proteins and virions, and propagate infection to healthy cells. Together, this study has revealed another route of apoptotic cell-phagocyte communication.

Rutter, S.F., Kang, T., Ryan, G.F. et al.
The formation of the ‘footprint of death’ as a mechanism for generating large substrate-bound extracellular vesicles that mark the site of cell death.
Nat Commun 16, 9160 (2025). https://doi.org/10.1038/s41467-025-64206-3

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Once again, we have a perfectly natural explanation for what creationists would call design if only the outcome were something they approved of. A complex cellular process, evolved for tissue maintenance and immune housekeeping, creates an opportunity which a virus can exploit. No intelligence is required; only variation, selection and the relentless opportunism of pathogens in their evolutionary arms race with their hosts.

But that leaves creationists with their familiar problem. If complexity, ingenuity and apparent purpose are evidence of design when they occur in an eye, a wing or a bacterial flagellum, then the same criteria must also apply to the machinery by which viruses invade, multiply and spread. The evidence does not change merely because the conclusion is theologically embarrassing. Either the designer designed both, or complexity is not evidence of design after all.

The usual escape route, of course, is to invoke 'Sin', 'The Fall' or some other item of Bronze Age mythology, but that is not science. It explains nothing, predicts nothing and adds nothing to our understanding of disease, immunity or evolution. It merely protects a cherished belief from evidence by moving the explanation out of reach of investigation.

Science, by contrast, follows the evidence wherever it leads. In this case, it leads not to a benevolent designer carefully arranging living things for human benefit, but to an evolved system full of trade-offs, vulnerabilities and historical compromises — exactly the sort of system we would expect from mindless evolution, and nothing like the flawless work of an omniscient, omnipotent and omnibenevolent god.

And once again, creationism is left not as an alternative explanation, but as a special pleading exercise: design when it flatters the myth, mystery when it does not, and denial when the evidence becomes too inconvenient to ignore.

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